Glaucoma in the Beagle is an inherited condition exhibited by open iridocorneal angles without gross anomalies. Intraocular pressure becomes elevated in Beagles 9 to 18 months of age. The outflow of aqueous humor, as measured serially by Schiotz and pneumatonograph tonography, is normal in young preglaucomatous Beagles but gradually decreases with the onset of glaucoma and thereafter. Buphthalmia is not obvious to casual inspection and by a-scan ultrasonography is limited to 1 to 2 mm anterioposteriorly. Lens dislocation and iridocorneal angle closure are directly related, occurring in about 30-month-old glaucomatous Beagles. Optic disk cupping and eventual atrophy occur as the disease advances. Glaucoma in the Beagle is inherited as an autosomal recessive trait. The disease has been reproduced in 74 Beagles. Selected matings to normal Beagles and subsequent back crosses to glaucomatous Beagles have established conclusively the mode of inheritance. The outflow of aqueous humor in glaucomatous Beagles is significantly less than control dogs, as estimated by tonography and constant pressure perfusion experiments. Light microscopic and SEM studies of early, moderate and advanced stages of this disease indicate a normal appearing iridocorneal angle that eventually closes. Evaluations of selected perfusates in the in vitro and in vivo normal canine eyes suggest perfusion rates are influenced directly by these substances. The in vivo and in vitro eyes also behave differently. Selected drugs including pilocarpine, carbonic anhydrase inhibitors, epinephrine and a carbachol derivative reduce intraocular pressure to a greater extent in the glaucomatous Beagle than laboratory quality Beagles.